Fig. 3

TRIM proteins in anti-HBV response of HCC. A PML is negatively correlated with HBsAg at the early-phase, because of proteasomal degradation and translocation to the nuclear. Down-regulated PML promotes apoptosis resistance and impairs DNA repair in HCC. B Long-term suppressed PML results in genome instability, which may confront the loss of HBV genes and HBsAg expression. However, PML turns out to be oncogenic since it enhances metabolic shift from glycogen storage to lipolysis. C TRIM22 is up-regulated under IFN stimulations. IFN activate IRF1, which is transferred to the nucleus and promote TRIM22 transcription by conjugating to its CpG island. D HBx suppresses IFN-induced transcription of TRIM22 gene through a single CpG methylation in its 5′-UTR, which reduces the IRF1 binding, thereby suppressing the IFN-stimulated induction of TRIM22 and exhibiting HBV immune escape. IRF1 IFN regulatory factor-1; HBx HBV regulatory protein X; UTR untranslated region